The Influence of Cations on Spontaneous and Chemically Induced Efflux of Noradrenaline from Perfused Rat Hearts

1972 ◽  
Vol 50 (6) ◽  
pp. 490-497 ◽  
Author(s):  
C. W. Nash ◽  
G. S. Taylor ◽  
T. E. Drouin
Keyword(s):  
Barium Ions ◽  
Efflux Of Noradrenaline ◽  
Chemically Induced ◽  
Rat Hearts ◽  
Na Efflux ◽  
Perfused Rat Hearts ◽  
Ca Ions ◽  
Storage Granules ◽  
Limited Supply ◽  
Na Release

Isolated rat hearts perfused with Krebs bicarbonate solution and labelled with 3H-noradrenaline (3H-NA) were used to study the influence of various cations on the efflux of noradrenaline from sympathetic nerve endings. Evidence is presented that EDTA causes release by influencing Mg more than Ca ions, possibly those associated in a Mg–ATPase complex at the storage granule. Calcium is required for release by excess potassium but inhibits release caused by BaCl2. In contrast to sustained increases in the rate of 3H-NA efflux caused by EDTA and noradrenaline, potassium and barium ions initiate short-duration increases which subside while the initiating agent is still present. It is postulated that potassium and barium may cause 3H-NA release from a limited pool of granules adjacent to the membrane or may make available a limited supply of intracellular free Ca ions to initiate release at the storage granules.

The Influence of Inorganic Ions on the Uptake and Retention of Tritiated Noradrenaline by Isolated Perfused Rat Hearts

1972 ◽  
Vol 50 (7) ◽  
pp. 645-654 ◽  
Author(s):  
C. W. Nash ◽  
T. Tu ◽  
M. J. Martin
Keyword(s):  
Extracellular Fluid ◽  
Inorganic Ions ◽  
Compartmental Analysis ◽  
Computer Assisted ◽  
Nonspecific Binding ◽  
Perfusion Fluid ◽  
High Sodium ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Ca Ions

The influence of a variety of modified Krebs media on the cumulative uptake of 3H-noradrenaline (3HNA) by perfused rat hearts was tested, and followed immediately by a determination of the effects of those altered media on the efflux of the tritiated compounds retained in the hearts. The efflux data were analyzed with the aid of a computer-assisted program for curve stripping and compartmental analysis, to indicate the distribution of 3HNA in the hearts. By this program the tritiated material in the heart was divided into four fractions: the nonspecific bound, the neuronal bound, the extraneuronal bound, and the free and loosely bound fractions. The results obtained from these experiments are summarized below. (1) Cocaine and desmethylimipramine reduced binding and passage of 3HNA into all cells, and in their presence the infused 3HNA was largely confined to the extra cellular space without uptake into tissue cells. (2) Reserpine prevented neuronal binding but the extraneuronal, the nonspecific, and the free and loosely bound fractions were also reduced, suggesting that reserpine may have some cocaine-like action. (3) Low calcium conditions increased uptake into the extraneuronal and the free and loosely bound fractions but reduced nonspecific binding. (4) EDTA reduced neuronal and extraneuronal binding but increased nonspecific binding and the amount in the free and loosely bound fraction. The effects of EDTA were similar to those of reserpine but had no cocaine-like action. (5) A high sodium concentration in the perfusion fluid increased binding in all fractions but under sodium-free conditions the neuronal and extraneuronal bound fractions were decreased while the nonspecific bound and the free and loosely bound fractions were increased. Neuronal binding required sodium but was not proportional to the concentration of sodium in the extracellular fluid. (6) Anions in the perfusion fluid influenced the uptake and distribution of 3HNA. Na2SO4 substituted for NaCl increased neuronal binding. NO3 and sodium cyanide substitution decreased neuronal binding but increased extraneuronal binding and the free and loosely bound fraction. The observations are consistent with the hypothesis that free Ca ions may inhibit transport and binding systems for noradrenaline in both nerve and extraneuronal tissues, probably largely muscle, and that alterations in the ionic environment which influence the availability of free Ca ions may influence the distribution of noradrenaline in perfused rat hearts.

Release of [3H]noradrenaline from perfused rat hearts by potassium and its modifications by 6-hydroxydopamine and reserpine

1976 ◽  
Vol 54 (6) ◽  
pp. 907-915 ◽  
Author(s):  
J. R. Carpenter ◽  
C. W. Nash
Keyword(s):  
Potassium Concentration ◽  
Cation Exchange Resin ◽  
Percentage Increase ◽  
Storage Vesicles ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Storage Granules ◽  
6 Hydroxydopamine ◽  
Almost All ◽  
Isolated Perfused Rat Hearts

The sources of noradrenaline (NA) released by excess potassium from isolated perfused rat hearts were investigated by labelling the hearts from normal, reserpine-treated, and 6-hydroxydopamine-treated (6-OHDA-treated) rats with [3H]NA, and measuring the increased rate of efflux induced by perfusion with a Krebs solution containing varying amounts of excess potassium. The [3H]NA and its metabolites in the effluent were separated by adsorption on alumina and a cation-exchange resin (Dowex-50). The release induced by potassium was a linear function of the log of the increased potassium concentration. Following a 1-h efflux period after labelling with [3H]NA, the hearts from reserpine-treated rats retained [Formula: see text] as much [3H]NA and released, in response to a 56 mM elevation in the potassium concentration, less than [Formula: see text] as much tritium label as the hearts from untreated (control) animals. In contrast, the hearts from 6-OHDA-treated animals retained [Formula: see text] of the amount of [3H]N A and released [Formula: see text] of the 3H label as did the control hearts. The potassium-induced increase of 3H-labelled substances in the effluent from the control hearts showed a large (threefold) percentage increase in the [3H]NA fraction, whereas the effluents from the hearts of reserpine- and 6-OHDA-treated animals contained only small increases in the [3H]NA fraction. Based on the assumptions that reserpine prevented retention of NA in the storage granules whereas 6-OHDA prevented almost all neuronal storage, it was concluded that more than 80% of the NA released by potassium excess from perfused normal hearts originated from the storage vesicles of the nerves, the remainder being largely from the cytoplasm of the nerves, with only a small portion from extraneuronal sources.

Effects of antiarrhythmic drugs on the extraneuronal accumulation of isoprenaline in perfused rat hearts

1986 ◽  
Vol 334 (2) ◽  
pp. 145-148 ◽  
Author(s):  
Kazumi Sono ◽  
Yoshinobu Akimoto ◽  
Kazuyoshi Kurahashi ◽  
Motohatsu Fujiwara
Keyword(s):  
Antiarrhythmic Drugs ◽  
Rat Hearts ◽  
Perfused Rat Hearts

Translocation of G-Protein β3 subunit from the cytosol pool to the membrane pool by β1-Adrenergic receptor stimulation in perfused rat hearts

1999 ◽  
Vol 58 (9) ◽  
pp. 1497-1500 ◽  
Author(s):  
Ken Kageyama ◽  
Takeshi Murakami ◽  
Kenji Iizuka ◽  
Kumi Sato ◽  
Kazuo Ichihara ◽  
...  
Keyword(s):  
G Protein ◽  
Adrenergic Receptor ◽  
Receptor Stimulation ◽  
Rat Hearts ◽  
Perfused Rat Hearts

Tm(DOTP)5−: A23Na+ shift agent for perfused rat hearts

1990 ◽  
Vol 15 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Douglas C. Buster ◽  
M. Margarida C. A. Castro ◽  
Carlos F. G. C. Geraldes ◽  
Craig R. Malloy ◽  
A. Dean Sherry ◽  
...  
Keyword(s):  
Rat Hearts ◽  
Perfused Rat Hearts
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